Bacteriophage P4 is a satellite of bacteriophage P2. It can replicate its own DNA and lysogenize its host, but it apparently carries no information for the structural proteins necessary for the construction of its virion. Instead, it relies on the genes of its helper phage P2 to supply that information. It is capable of activating the necessary genes of its helper, and in so doing, causes the condensation of a capsid 1/3 the size of that produced by the helper itself. This proposal is concerned with the mechanism by which P4 induces the condensation of the smaller capsids. The elucidation of this mechanism will allow insight into the morphogenic pathway of icosahedral capsid construction and the assembly of other complex biological structures. P4 relieves the strong polarity of amber mutations in helper operons. A mutant of P4, P4 sid 1, which has lost the ability to produce small capsids, also has lost this ability to suppress polarity. P4 sid 1 or P2 solo infection of a rho (transcription termination defective) strain yields a majority of small capsids suggesting that termination of transcripts plays a regulatory role in capsid size determination. It is proposed to: a) utilize electron microscopic examination of R loops in P2 DNA generated from RNA extracted from phage-infected cells to determine if the presence of P4 results in enhanced production of mRNA in promoter distal portions of P2 operons; b) measure the capsid sizes produced by P2 in a spectrum of rho mutants to see if the size-determining effect is allele-specific; c) vary the ratios of various P2 gene products by the use of amber mutants and a temperature-sensitive amber suppressor to determine which gene products determine capsid size; and d) infect other phages into the above rho mutants and examine the structures produced to see if this method of regulation is a general one.